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Infective Endocarditis
DR. MOSTAFA ALSHAMIRI ASSOCIATE PROFESSOR CONSULTANT CARDIOLOGIST HEAD OF ADULT CARDIOLOGY Director of Coronary Care KING FAHED CARDIAC CENTER 341, KKUH October, 2018
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AGENDA Definition Path-physiology The risk factors Clinical features
Diagnosis Treatment Complication Prevention
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Infective Endocarditis
Definition : Infection of endothelium surface of heart either of 1. Heart valves . 2. Septal defects. 3. Chordae Tontine . 4. A.V shunt. It remains a life-threatening disease with significant mortality (about 20%) and morbidity.
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Pathogenesis of IE-1 The IE is the net result of the complex interaction between the bloodstream pathogen with matrix molecules and platelets at sites of endocardial cells damage.
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Pathogenesis of IE-2 Endothelial damage Turbulent blood flow produced by certain types of congenital or acquired heart disease, such as flow from a high- to a low-pressure chamber or across a narrowed orifice, traumatizes the endothelium. Formation of nonbacterial thrombotic endocarditis ( NBTE ) Endothelial damage creates a predisposition for deposition of platelets and fibrin on the surface of the endothelium, which results in NBTE. Bacteremia Invasion of the bloodstream with a microbial species that has the pathogenic potential to colonize this site ,then result in Proliferation of bacteria within a vegetation and form IE.
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Pathogenesis of IE-3 Transient Bacteremia Mucosal surfaces are populated by : Dense endogenous microflora. Trauma to a mucosal surface like: Gingiva around teeth, Oro-pharynx, GI tract, Urethra, Vagina, This will releases many different microbial species transiently into the bloodstream which will leads to Transient bacteremia caused by organism e,g Veridans group streptococci
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Pathogenesis: summery-1
1.High velocity jet 2.Flow from high pressure to low pressure chamber 3.Flow across narrow orifice of high velocity Endothelial damage Platelet-fibrin thrombi (Nonbacterial Thrombotic endocarditis) Mucosal surface damage - dental Microorganism adherence (BTE) Local vegetation EXTENSON , Perivalvular ,Destructive valve, fistula and embolization
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Determining Risk of IE Cardiac conditions Type of Procedure
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Cardiac Conditions – High Risk1
Old recommendation Prosthetic Valves (400x risk2) Previous endocarditis Congenital heart disease Complex cyanotic disease (Tetralogy, Transposition, Single Ventricle) Patent Ductus Arteriosus VSD Coarctation of aorta Valvular: not included as per now Aortic Stenosis/ Aortic Regurgitations Mitral Regurgitation Mitral Stenosis with Regurgitations 1Durack, et al. NEJM 1995 Mod Risk per 1997 AHA guidelines 2Steckleberg, et al. Inf Dis Clin N Amer 1993
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2015 recommendations
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2015 recomendations
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Prophylaxis against IE ACC 2017
Is reasonable before dental procedures that involve manipulation of: gingival tissue, peri-apical region of teeth, or perforation of the oral mucosa in patients with the following: 1. Prosthetic cardiac valves, including trans-catheter-implanted prostheses & homografts. 2. Prosthetic material used for cardiac valve repair, such as annuloplasty rings & chords. 3. Previous IE. 4. Unrepaired cyanotic congenital heart disease or repaired congenital heart disease, with residual shunts or valvular regurgitation at the site of or adjacent to the site of a prosthetic patch or prosthetic device. 5. Cardiac transplant with valve regurgitation due to a structurally abnormal valve.
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CLASSIFICATION OF ie Type of lesion Native. Congenital Prosthetic.
Onset & progress Acute. Sub acute. Acquire of infection Nosocomial . community
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DIAGNOSIS OF IE Clinical suspension Blood culture Echocardiography
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Clinical Features-1 › Indolent course: -fever - Malaise
Onset usually within 2 weeks of infection › Indolent course: -fever - Malaise - Fatigue - Night sweats - Anorexia - Weight loss › Explosive course: - CCF , murmur new onset or changing characters, with severe systemic sepsis
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Other Clinical Features-2
Spleno-megaly ~ 30% Petechiae % Conjunctivae Buccal mucosa palate Skin in supra-clavicular regions Osler’s Nodes % Splinter Haemorrhages % Roth Spots ~ 5% Musculoskeletal (arthritis)
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Vascular and septic emboli
Immonuligical Vascular and septic emboli Osler nodes Roth spot Gomeriolo-nephritis Rheomatoid factor + Splinter hemorrhage Janway lesion : painless skin lesion in the palm and sole. Sub-conjuctival hemorrhage Mycotic aneurysm Arthritis hematurea
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Clinical features- immunological phenomina (glumerolo-nephriti, osler nodes, roth spot , RF +ve)
Osler nodes , painful lesion in distal finger
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Roth Spots
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Vascular Phenomina -Septic emboli
Janway , vascular Painless hemorrhagic cutaneus lesion in the palm and sole Splinter hg
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Subconjunctival Hemorrhages
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AA common mnemonic for the signs and symptoms of endocarditis is FROM JANE:
F- FEVER R- ROTH SPOT O- OSLER NODE M- MURMER J- JEANWAY LESION A- ANEMIA N- NAIL HG (SPLINTER HG) E- EMBOLI
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INVESTIGATIONS C.B.C ESR Blood cultures RFT URINE ECG CXR ECHO
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TEE
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Skin most predominant source of infection
IE in IV Drug Abusers Skin most predominant source of infection % of Rt. sided IE results in pneumonia and septic emboli Microbiology Staph aureus ~60% Streptococci and Enterococci ~20% Gram -ve bacilli ~10% Fungi (Candida and Aspergillus ~5%
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Prosthetic Valve Endocarditis Classification
Early ( < 60 days ) Reflects perioperative contamination Incidence around 1% Microbiology Staph ( %) Staph. Epiderm (~ 30%) Staph. Aureus (~ 20%) Gram -ve aerobes (~20%) Fungi (~ 10%) Strep and Entero (5-10%) Late ( > 60 days) After endothelialization Incidence % / pt. year Transient bacteraemia from dental, GI or GU Microbiology resembles native valve endocarditis
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DUKE CRITERIA BE-FEVEER(SUMMARY)
MAJOR B-BLOOD CULTURE +VE >2 TIMES 12 HOUR APART E- ENDOCARDIAL INVOLVEMENT FROM ECHO MINOR CRITERIA F- FEVER E- ECHO FINDING NOT MAJOR V- VASCULAR PHENOMINA EE- EVIDENCE FROM MICROBIAL /IMMUNOLOGICAL- 2 EVIDENCE R- RISK FCTOR FOR IE VALVE DISEASE /CONGEITAL DRUG ABUSER
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Diagnostic (Duke) Criteria
Definitive infective endocarditis Pathologic criteria Microorganisms or pathologic lesions: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess Clinical criteria (as above) Two major criteria, or One major and three minor criteria, or Five minor criteria
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Diagnostic (Duke) Criteria
Possible infective endocarditis findings consistent of IE that fall short of “definite”, but not “rejected” IE considered in presence of 1 major + 1 minor or 3 minor Rejected Firm alternate Dx for manifestation of IE Resolution of manifestations of IE, with antibiotic therapy for 4 days No pathologic evidence of IE at surgery or autopsy, after antibiotic therapy for 4 days
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Treatment Medical – antibiotic Surgical
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Principles of Medical Management
Antibiotic needs : prolonged , high dose and bactericidal. Acute onset: blood culture and start treatment within three hours. Sub acute onset ; Blood culture then antibiotic can be started within three days.
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Treatment Pre-antibiotic era - a death sentence Antibiotic era
Microbiologic cure in majority of patient Highly penicillin-susceptible Streptococcus viridans or bovis Once-daily ceftriaxone for 4 wks cure rate > 98% Once-daily ceftriaxone 2 g for 2wks followed by oral amoxicillin qid for 2 wks Prosthetic valve may need longer treatment durations.
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Complications-1 Congestive Cardiac Failure (Commonest complication)
Valve Destruction Myocarditis Coronary artery embolism and MI Myocardial Abscesses Neurological Manifestations (1/3 cases) Major embolism to MCA territory ~25% Mycotic Aneurysms %
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Neurological Complication
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Complications-2 Metastatic infections Rt. Sided vegetations
Lung abscesses Pyothorax / Pyo-pneumothorax Lt. Sided vegetations Pyogenic Meningitis Splenic Abscesses Pyelonephritis Osteomyelitis Renal impairment , Glomerulonephritis
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Prevention
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Staphylococcus Flocloxacilline Or Vancomycine
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